The fate of chondrocytes during cartilage erosion in the growing tibia in the domestic fowl (Gallus domesticus).
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The middle cardiac nerve, a branch of the vagus, innervates the ventricles of the avian heart. Of 533 myelinated sensory fibers, the size range was 2 micron. The ratio of myelinated to unmyelinated sensory fibers ranged from 2.17 to 3.48. Sensory endings resembled a network pattern with no distinct receptor-like endings. Frequency of nerve population increased from apex to base of the heart.
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1. In order to quantify losses of Na and K associated with precipitate fractions in semi-solid avian urines, Na, K, uric acid and urates (UA + U) and inulin were measured in plasma, in whole ureteral urine, and in urinary precipitates of hens. Ten animals were used, five fed a control commercial poultry meal (Diet A) and five maintained on a high protein, low-Na feed (Diet B). 2. In ureteral urines from hens on Diet A, dried precipitate accounted for 5.6% of the total whole urine weight, on the average. UA + U constituted about two-thirds of the precipitates' weight and 80% of the total excreted UA + U load of 97.4 mM. The average molar fractions, [Na]/[UA + U] and [K]/[UA + U], in precipitates were in the range 0.1-0.2; and the Na and K lost in these fractions were 12.8 mequiv and 9.6 mequiv, respectively, per 1 whole urine. These losses represent 9% and 23% of total Na and K excretion. 3. Diet B was used to accentuate potential cation loss in precipitates if obligatory binding of K and especially Na were to occur in precipitates. Urinary [UA + U] in whole urine rose to 146 mM of which 95% was found in precipitates. The average molar fraction [Na]/[UA + U], however, fell to 0.06 and that of [K]/[UA + U] to 0.08. Renal loss of Na was 8.5 mequiv and of K was 11.5 mequiv per 1 whole urine. 4. These experiments reveal that significant but minor fractions of excreted Na and K are associated with precipitates of avian urine, although the loss is insignificant compared to that reported in starlings (Braun, 1978). They further indicate that the Na/inulin clearance ratio, based on measurements in whole urine and plasma, adequately reflects fractional excretion which, on Diet A, was 1.8% of the filtered load and, on the Na-poor Diet B, less than 0.1%. These values place the Na-reabsorbing abilities of these birds easily within the range reported for ureotelic vertebrates and suggest that uricotelism does not impose a major renal salt loss in birds.
1. In order to assess the role of uricotelism in net renal acid excretion, blood and ureteral urine samples were collected from five hens fed a commercial poultry feed (Diet A) and five hens fed a protein-rich, Na-poor feed (Diet B). All samples were analysed for pH, PCO2, ammonium, phosphate, uric acid and urates (UA + U) and inulin. 2. On Diet A, average pH in venous blood was 7.42, while urinary pH (pHu) ranged from 4.74 to 7.25. At average pHu (6.10), uric acid accounted for 52% of total acid excreted, H2PO4 for 20% and NH4 for 28%. Net acid excretion in ureteral urine was 345 muequiv h-1 kg body weight-1, or 5-10 times that observed in ureotelic vertebrates (amphibians and mammals). 3. The relative contributions of these urinary buffers to net renal acid excretion changed with pHu. Significant negative correlations exist between pHu and both total phosphate and ammonium excretion rates (P less than 0.001). Excretion rates of (UA + U) showed a positive correlation (P less than 0.05) with pHu. 4. Feeding on Diet B revealed the homeostatic power of the avian kidney. Blood pH and PCO2 were not changed relative to values in hens fed the control diet while striking increases in excretion rates of all urinary buffers (except HCO3) were observed. Average pHu fell to 5.12, and the average net renal acid excretion rate doubled.
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The effects of gamma amino butyric acid (GABA), bicuculline and amino-oxyacetic acid (AOAA) on nitrazepam-induced sleep were studied in young chicks. GABA (200-3200 mg/kg) induced a marked sedation in young chicks. It also potentiated nitrazepam (1.6 mg/kg)-induced sleep. Bicuculline (1.25-5.00 mg/kg) effectively antagonized nitrazepam-induced sleep. In addition, it effectively antagonized GABA (1600 mg/kg)-induced potentiation of nitrazepam sleep. AOAA (2.5-7.5 mg/kg) delayed the onset of nitrazepam sleep, but significantly prolonged its duration. Nitrazepam (1.6 mg/kg) synchronized the electroencephalogram (EEG) of the hyperstriatum, optic tectum and reticular formation. Similarly, the electromyograph (EMG) activity was markedly reduced. GABA (1600 mg/kg) synchronized the EEG of the hyperstriatum, optic tectum and reticular formation while the EMG activity was reduced. Administration of GABA (1600 mg/kg) into nitrazepam (1.6 mg/kg)-pretreated chicks induced desynchronization of the EEG of the hyperstriatum, while the EEG of the reticular formation was synchronized. In addition, the EMG activity was reduced. Bicuculline (5 mg/kg) activated the EEG of the hyperstriatum; this effect was antagonized by GABA (1600 mg/kg). Similarly, GABA (1600 mg/kg)-induced decrease in EMG activity, synchronization of the EEG of the optic tectum and reticular formation was antagonized by bicuculline. The present data suggest that GABA potentiated nitrazepam-induced behavioral and electroencephalographical sleep.